We developed a model system that eliminated eggs of Schistosoma mansoni as a factor of pathological consideration and amplified the pathological effects of preadult schistosomes. After a single, massive exposure of mice to cercariae of S. mansoni, worms did not reach sexual maturity, and the mice died before the onset of deposition of eggs. Mice exposed to 3,000 cercariae did not survive past the 4th week after exposure. Development of the schistosome population was retarded. Histopathological findings showed areas of necrosis in the liver, but they were not universally associated with prepatent mortality. Infected mice showed a loss of body weight at death, apparently caused by inhibition of feeding owing to reduction in locomotor activity before death. Physiological evidence obtained with uninfected, starved mice suggests that death of infected mice was not solely the result of weight loss. The absence of portal hypertension indicated that death during prepatency was not the result of blockage of the hepatic portal system by developing schistosomes. Body temperature and cardiac rate decreased concomitantly in infected mice over a 24-hour period, until death finally occurred.
Present address: Laboratory of Parasitology, Department of Biology, Tulane University, New Orleans, Louisiana 70118.